Atrial natriuretic factor (ANF), a peptide 'hormone', isolated from atria and hypothalamus, is a potent vasodilator and natriuretic factor. ANF has physiopathologic implications in hypertension, congestive heart failue, and expansion of blood volume. Studies have demonstrated that vasopressin acts to increase the secretion of ANF. Other studies have demonstrated that the administration of ANF attenuates the increase in vasopressin induced by hemorrhage and water deprivation. Thus, it appears that both ANF and vasopressin are components of a negative feedback control system. The hypothesis of the proposed studies is that the action of ANF that inhibit vasopressin secretion is mediated by tuberohypophyseal dopaminergic (THDA neurons in the hypothalamus. We propose that ANF, from either atrial or hypothalamic sites, stimulates the activity of THDA neurons. THDA neurons, in turn, act to inhibit vasopressin secretion. Vasopressin, released into the systemic circulation or via axon collaterals in the hypothalamus, acts to stimulate the secretion of ANF. The proposed studies will utilize neurochemical and radioimmunoassay procedures and were designed to determine if: 1) ANF stimulates the activity of THDA neurons, 2) THDA neurons mediate the ANF-induced inhibition of vasopressin secretion, 3) vasopressin stimulates ANF secretion and THDa neuronal activity, 4) exogenous vasopressin inhibits the hemorrhage- and dehydration-induced increase in endogenous vasopressin secretion 5) vasopressin mediates the hemorrhage- and dehydration-induced increases in ANF secretion and THDA neuronal activity, 6) ANF mediates the hemorrhage- and dehydration-induced increases in THDA neuronal activity.